Exposure to cues associated with palatable food reward results in a dopamine D2 receptor-dependent suppression of evoked synaptic responses in the entorhinal cortex

Hutter, Juliana A.; Chapman, C. Andrew

doi:10.1186/1744-9081-9-37

Cited by 5 publications

(4 citation statements)

References 55 publications

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“…Additionally, rotenone plus REMSD led to a drastic reduction in the number of rescued TH-ir neurons, most likely by the D2 agonist piribedil. These data are in accordance with previous reports that also described the involvement of the dopaminergic system in olfaction (Mundiñano et al, 2011 ; Hutter and Chapman, 2013 ; Borghammer et al, 2014 ). We suppose that the increased olfactory TH-ir neurons that we observed following rotenone treatment might be the result of phenotypic and perhaps epigenetic changes in pre-existing olfactory GABAergic neurons.…”

Section: Discussionsupporting

confidence: 93%

Olfactory impairment in the rotenone model of Parkinsonâ€™s disease is associated with bulbar dopaminergic D2 activity after REM sleep deprivation

Rodrigues

Targa

Noseda

et al. 2014

Front. Cell. Neurosci.

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Olfactory and rapid eye movement (REM) sleep deficits are commonly found in untreated subjects with a recent diagnosis of Parkinson’s disease (PD). Additionally, different studies report declines in olfactory performance during a short period of sleep deprivation. Mechanisms underlying these clinical manifestations are poorly understood, and impairment of dopamine (DA) neurotransmission in the olfactory bulb and the nigrostriatal pathway may have important roles in olfaction and REM sleep disturbances. Therefore, we hypothesized that modulation of the dopaminergic D2 receptors in the olfactory bulb could provide a more comprehensive understanding of the olfactory deficits in PD and REM sleep deprivation (REMSD). We decided to investigate the olfactory, neurochemical, and histological alterations generated through the administration of piribedil (a selective D2 agonist) or raclopride (a selective D2 antagonist) within the glomerular layer of the olfactory bulb, in rats subjected to intranigral rotenone and REMSD. Our findings provide evidence of the occurrence of a negative correlation (r = −0.52, P = 0.04) between the number of periglomerular TH-ir neurons and the bulbar levels of DA in the rotenone, but not sham, groups. A significant positive correlation (r = 0.34, P = 0.03) was observed between nigrostriatal DA levels and olfactory discrimination index (DI) for the sham groups, indicating that increased DA levels in the substantia nigra pars compacta (SNpc) are associated with enhanced olfactory discrimination performance. Also, increased levels in bulbar and striatal DA were induced by piribedil in the rotenone control and rotenone REMSD groups, consistent with reductions in the DI. The present evidence reinforce the idea that DA produced by periglomerular neurons, particularly the bulbar dopaminergic D2 receptors, is an essential participant in olfactory discrimination processes, as the SNpc, and the striatum.

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Section: Discussionsupporting

confidence: 93%

Olfactory impairment in the rotenone model of Parkinsonâ€™s disease is associated with bulbar dopaminergic D2 activity after REM sleep deprivation

Rodrigues

Targa

Noseda

et al. 2014

Front. Cell. Neurosci.

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“…Corroborating other studies, which also evaluated the participation of the dopaminergic system in the olfactory function 24 , 31 , 49 , 50 , rotenone alone, appears to consistently reduce the DI in both social and non-social odor (lemon). Even more recently, it has been demonstrated, the existence of a direct dopaminergic projection, from the SNpc to the olfactory bulb, probably influencing olfactory performance, particularly in PD 32 .…”

Section: Discussionsupporting

confidence: 59%

Olfactory impairment is related to REM sleep deprivation in rotenone model of Parkinson's disease

et al. 2017

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IntroductionOlfactory dysfunction affects about 85-90% of Parkinson's disease (PD) patients with severe deterioration in the ability of discriminate several types of odors. In addition, studies reported declines in olfactory performances during a short period of sleep deprivation. Besides, PD is also known to strongly affect the occurrence and maintenance of rapid eye movement (REM) sleep.MethodsTherefore, we investigated the mechanisms involved on discrimination of a social odor (dependent on the vomeronasal system) and a non-social odor (related to the main olfactory pathway) in the rotenone model of PD. Also, a concomitant impairment in REM sleep was inflicted with the introduction of two periods (24 or 48 h) of REM sleep deprivation (REMSD). Rotenone promoted a remarkable olfactory impairment in both social and non-social odors, with a notable modulation induced by 24 h of REMSD for the non-social odor.ResultsOur findings demonstrated the occurrence of a strong association between the density of nigral TH-ir neurons and the olfactory discrimination capacity for both odorant stimuli. Specifically, the rotenone-induced decrease of these neurons tends to elicit reductions in the olfactory discrimination ability.ConclusionsThese results are consistent with the participation of the nigrostriatal dopaminergic system mainly in the olfactory discrimination of a non-social odor, probably through the main olfactory pathway. Such involvement may have produce relevant impact in the preclinical abnormalities found in PD patients.

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“…Consistent with the connectivity in this network (McDonald, 1984;Bell-McGinty et al, 2002), the impact of the BLA on the manifestation of depressive symptoms appears to be mediated by the LEC (during positive false recognition) and DG/CA3 (during neutral discrimination), implicating a particular amygdala-hippocampal pathway in depression. Selectivity of network dysfunction during positive false recognition in late-life depression may be due to the LEC's connection with ventral tegmental area dopamine neurons, which are associated with reward-related stimuli (Hutter and Chapman, 2013;Dillon, 2015). Furthermore, the "positivity effect" reported in aging (Mather and Carstensen, 2005) and a recent study from our lab showing the positivity effect is specific to older adults with age-related memory impairment (Leal et al, 2016a) suggests that older adults with depression may have hippocampal and entorhinal hyperactivity during positive false recognition that may underlie deficits in remembering positive information in depression (Dillon, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…It is interesting that we only see differences in positive lure processing during false recognition, when participants are incorrectly discriminating a positive lure item, suggesting these signals may be partially responsible for positive memory deficits observed in depressed individuals. While this remains speculative, it is possible that the LEC showed a unique activity profile for positive stimuli at least in part due to its connection with ventral tegmental area (VTA) dopamine neurons, which are associated with reward-related stimuli (Hutter and Chapman, 2013;Dillon, 2015).…”

Section: Increased Hippocampal and Lec Signals During Positive False Recognition In Older Adults With Depressive Symptomsmentioning

confidence: 99%

Disruption of amygdala–entorhinal–hippocampal network in late‐life depression

et al. 2017

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Episodic memory deficits are evident in late-life depression (LLD) and are associated with subtle synaptic and neurochemical changes in the medial temporal lobes (MTL). However, the particular mechanisms by which memory impairment occurs in LLD are currently unknown. We tested older adults with (DS+) and without (DS-) depressive symptoms using high-resolution fMRI that is capable of discerning signals in hippocampal subfields and amygdala nuclei. Scanning was conducted during performance of an emotional discrimination task used previously to examine the relationship between depressive symptoms and amygdala-mediated emotional modulation of hippocampal pattern separation in young adults. We found that hippocampal dentate gyrus (DG)/CA3 activity was reduced during correct discrimination of negative stimuli and increased during correct discrimination of neutral items in DS+ compared to DS- adults. The extent of the latter increase was correlated with symptom severity. Furthermore, DG/CA3 and basolateral amygdala (BLA) activity predicted discrimination performance on negative trials, a relationship that depended on symptom severity. The impact of the BLA on depressive symptom severity was mediated by the DG/CA3 during discrimination of neutral items, and by the lateral entorhinal cortex (LEC) during false recognition of positive items. These results shed light on a novel mechanistic account for amygdala-hippocampal network changes and concurrent alterations in emotional episodic memory in LLD. The BLA-LEC-DG/CA3 network, which comprises a key pathway by which emotion modulates memory, is specifically implicated in LLD.

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Exposure to cues associated with palatable food reward results in a dopamine D2 receptor-dependent suppression of evoked synaptic responses in the entorhinal cortex

Cited by 5 publications

References 55 publications

Olfactory impairment in the rotenone model of Parkinsonâ€™s disease is associated with bulbar dopaminergic D2 activity after REM sleep deprivation

Olfactory impairment in the rotenone model of Parkinsonâ€™s disease is associated with bulbar dopaminergic D2 activity after REM sleep deprivation

Olfactory impairment is related to REM sleep deprivation in rotenone model of Parkinson's disease

Disruption of amygdala–entorhinal–hippocampal network in late‐life depression

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